Parasites may seem too gross or too wicked to be worth saving from extinction. Or they may just seem so skilled in their sinister arts that we don’t have to worry about them, since they’ll always find a new victim.

In fact, parasites warrant our concern, right along with their hosts. That’s not to say that we’d better off if smallpox or rinderpest were still running wild. But letting parasites hurtle into oblivion due to our ecological recklessness is a bad idea.

Here’s a case in point: The World Wildlife Fund has just drawn attention to a parasitic wasp, Ampulex dementor, that makes cockroaches its zombified victims. The wasp was found in 2007 in Thailand, and in 2014 a German museum held a contest to give it a species name. Museum goers voted to name it after the soul-sucking dementors in the Harry Potter series.

WWF highlighted A. dementor in a new report on the 139 new species from the Greater Mekong Region that were described in 2014 alone. This region, which includes Cambodia, Laos, Myanmar, Thailand, and Vietnam, is stunningly rich with species. It’s also incredibly productive, yielding a quarter of the world’s catch of freshwater fish. But it’s also under intense pressure, ranking in the top five threatened biodiversity hotspots on Earth. Dams, roads, logging, and hunting are all taking their toll on the species there. Climate change will only add to the threats the Mekong’s species face.

A species like A. dementor is caught in a special bind. We didn’t even know it existed until recently, so it’s hard to know precisely how well the species is faring. No one has a detailed map of its range before human pressure ramped up in the past century, and no one has a corresponding map of its current range.

On top of that, the published scientific literature–pretty much just a single paper published last year–doesn’t even tell us about the particular cockroaches the wasp parasitizes. Does it zombify several species of cockroaches? Does it zombify just one? These questions matter a lot to the survival of A. dementor. If it parasitizes a single rare species, it could become extinct if its host disappears. (While a few species of cockroaches have become global champions by adapting to our homes, the vast majority can only survive in wild forests.)

While we know little about this parasite, the ecological threats to the Greater Mekong Region should make us concerned about it. And losing a species of parasite can be a bad thing. Parasites, for example, are important players in food webs. If they disappear from an ecosystem, their hosts–and the species that are affected by those hosts–may undergo wild swings. If you don’t like cockroaches, the last thing you want is for the parasites that devour them from the inside out to vanish.

Parasites are also worth saving for what they have to teach us. And that’s especially true for wasps like A. dementor. It belongs to a lineage known as Ampulicidae or the cockroach wasps, which contains 200 named species–and probably many more waiting to be discovered. The best known of these species is Ampulex compressa, sometimes called the emerald cockroach wasp. Phenomena readers may be quite familiar with the emerald cockroach wasp, because fellow blogger Ed Yong and I just won’t shut up about it. (I also added an epilogue to my book Parasite Rex pretty much just to write about it.)

The reason we know so much about the emerald cockroach wasp is that a team of researchers led by Frederic Libersat at Ben-Gurion University in Israel have figured out how to rear the wasps in their lab, and for years now they’ve been observing its remarkable skills.

The female emerald cockroach wasp searches for roaches, probably scanning the ground while sniffing the air. The wasp swoops down on the roach and stings it in its abdomen, temporarily paralyzing it. It then delivers a second shot to the head–literally snaking its stinger into the recesses of the cockroach brain. Now the cockroach loses all motivation to do much of anything. You can even shock its leg and it won’t budge on its own. But the wasp can grab onto an antenna and lead it into a burrow.

There, the wasp lays an egg on the roach’s underside and then leaves, sealing the burrow behind it. The egg hatches and the larva sucks on the roach in tick-like fashion for a while, before squirming inside the host’s body to finish off its growth. To keep its host from dying of infections, it smears an antibiotic cocktail on the roach’s inner body wall. The wasp larva forms a cocoon inside the roach, which then finally dies. Later, the fully-grown wasp pokes its head out of the roach, wriggles entirely free, and leaves the burrow.

These wasps may have many lessons for us. Most of their antibiotics are new to science, for example, and so they may be worth investigating further for medicine. The wasps have also evolved a remarkable skill at manipulating the cockroach brain. Figuring out how they do it might tell us more about how the nervous systems of insects work. And it might provide some inspirations for ways to manipulate our own brains–not to turn ourselves into zombies, but to treat psychological disorders.

But almost all the insights we’ve got about cockroach wasps come from a single species. Far from being degenerates, as they were traditionally viewed, parasites can evolve rapidly, hitting on new strategies for conquering their hosts. So it’s entirely possible that A. dementor uses a soul-sucking arsenal that’s significantly different than its cousin species A. compressa. The only way we can enjoy discovering that arsenal is to make sure this species doesn’t vanish first.

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If you want to find out more about cockroach wasps, here are some pointers:

Parasites are life’s great success story, abundant in both species and sheer numbers. One secret to their success is the ability that many parasites have to manipulate their hosts. By pulling strings like a puppet master, they use their hosts to advance towards their own goal of planetary conquest. Creepy is the best word to describe most of their strategies. They turn some hosts suicidal. They castrate others. They turn still others into zombie bodyguards. But a new study published today suggests that the parasite that causes malaria may use a more pleasant strategy. It lures mosquitoes to infected hosts with a lemony scent.

Malaria is caused by single-celled parasites called Plasmodium. A female mosquito carries them in its gut as it flies around in search of a victim to bite. After the parasites mature, they push through the insect’s gut wall, eventually making their way into its salivary glands. When the mosquito lands on a person and drills into the skin, it pushes some of its Plasmodium-laden saliva into the wound.

The parasites now begin their long journey through the human body. They get pushed by the surges of the bloodstream to the liver, where they invade cells and multiply inside them. The infected liver cells erupt with the next stage of Plasmodium’s life cycle, called merozoites. The merozoites end up back into the bloodstream, where they now invade red blood cells. They multiply yet again, rupturing the blood cells and invading new ones. Eventually the parasites achieve the next stage in their life cycle, when they’re ready at last to get sucked up by a hungry mosquito in a meal of blood.

If Plasmodium can’t get into a mosquito, all of this multiplication is for naught. So anything that the parasite can do to increase the odds of a successful exit can potentially be favored by natural selection. Last year, for example, a team of researchers found that mosquitoes were attracted to mice infected with Plasmodium parasites–but only when they were ready to leave their rodent host. The scientists found evidence that the parasites engineer this attraction by changing the odor of the mice. Infected mice give off odor molecules that draw mosquitoes to them.

Those scientists speculated that perhaps the parasite alters its hosts chemistry to make new odors. But recently Audrey Odom of Washington University and her colleagues raised another possibility: maybe the parasites themselves produce mosquito-attracting chemicals.

Other scientists had explored this possibility before without much to show for their efforts. But Odom and her colleagues suspected that previous researchers hadn’t looked hard enough. So the Washington University team added Plasmodium to much larger volumes of blood than before–400 milliliters–and then snagged odors rising off the blood with more sensitive traps. The efforts paid off: Odom and her colleagues found that when Plasmodium infected red blood cells, it produced chemicals called pinene and limonene.

You have probably smelled these chemicals before. Pinene is part of the blend of odors that make up the scent of pine trees. Limonene gets its name from lemons, which produce it in their rinds.

If you’re confused at this point about a single-celled blood parasite producing a fragrant odor, you have every right to be. To make sense Odom’s weird discovery, we have to take a sharp detour through more than a billion years of evolution.

It’s 1.3 billion years ago. The planet is ruled by bacteria and protozoans. Animals and plants won’t evolve for many hundreds of millions of years. On the surface of the ocean, some bacteria are capturing sunlight with photosynthesis, while protozoans are preying on them. Somehow, this story goes off-script, and some protozoans end up with photosynthetic bacteria trapped inside them. Instead of becoming food, the bacteria supply the food, powering the protozoans with photosynthesis. Over many generations, the bacteria become an inseparable part of their host. The combination of these two kinds of life become a new kind, which we call algae.

This primordial algae had many descendants. Some of them evolved into green algae, and eventually gave rise to plants on land. Another lineage of algae were swallowed up by yet another protozoan, and became another form of algae found on Earth today, known as red algae. Some red algae live now as free-floating photosynthesizers in the ocean. Others took up inside corals, providing coral animals with sustenance from the sun. And still other red algae became parasites of animals. Some of these parasites eventually became Plasmodium.

Plasmodium’s ancestors lost the ability to photosynthesize a long time ago. But they still hold onto some of the ancestral enzymes from the bacteria that their forebears swallowed 1.3 billion years ago. As a result, Plasmodium is weirdly similar to flowers and trees. Some scientists have even taken advantage of this evolutionary kinship by looking at weed-killers as potential drugs for malaria.

This ancient heritage also explains why Plasmodium can smell like lemons. Odom and her colleagues found that the parasite make pinene and limonene using enzymes that are related to the ones that plants use to make these chemicals.

There are reasons to think that the parasite are using these chemicals to lure mosquitoes. While we’re painfully aware of the appetite mosquitoes have for blood, the fact is that mosquitoes also feed on flower nectar. They depend on the nectar for sugar they need to fuel their flights. Many insects are keenly sensitive to certain colors and odors that flowers produce, which guide them reliably to their next meal of nectar. Odom and her colleagues found that the antenna of malaria-carrying species of mosquitoes are exquisitely sensitive to pinene and limonene. If you want to attract mosquitoes, it makes sense to make those chemicals.

While this research is tantalizing, it is only the first step in testing the hypothesis that Plasmodium makes a fragrant odor to lure its next host. So far, Odom and her colleagues have only demonstrated that the parasites are making these chemicals inside red blood cells. It’s certainly conceivable that in a living host, these odors could escape into the lungs and leave the body with exhaled air. It remains to be seen if they really do get out, and if they make a difference to the success of Plasmodium. Or perhaps this parasite perfume has some other function, and it remains bottled up inside sick hosts.

(For more examples of parasite manipulation, see my cover story in the November 2014 issue of National Geographic or my book Parasite Rex.)

In November, National Geographic put a ladybug and a wasp on its cover. They made for a sinister pair. The wasp, a species called Dinocampus coccinellae, lays an egg inside the ladybug Coleomegilla maculata. After the egg hatches, the wasp larva develops inside the ladybug, feeding on its internal juices. When the wasp ready to develop into an adult, it crawls out of its still-living host and weaves a cocoon around itself.

As I wrote in the article that accompanied that photograph, the ladybug then does something remarkable: it becomes a bodyguard. It hunches over the wasp and defends it against predators and other species of parasitic wasps that would try to lay their eggs inside the cocoon. Only after the adult wasp emerges from its cocoon does the bodyguard ladybug move again. It either recovers, or dies from the damage of growing another creature inside of it.

How parasites turn their hosts into zombie slaves is a tough question for scientists to answer. In some cases, researchers have found evidence suggesting that the parasites release brain-controlling chemicals. But the wasp uses another strategy: there’s a parasite within this parasite.

In the Proceedings of the Royal Society, a team of French and Canadian researchers now lay out the evidence for this strange state of affairs. As they studied this manipulation, they reasoned that the best place to look for clues was inside the heads of parasitized ladybugs. They discovered that the brains of these hosts were loaded with viruses. When the scientists sequenced the genes of the virus, they found it was a new species, which they dubbed D. coccinellae Paralysis Virus, or DcPV for short.

The scientists found DcPV in the wasps as well–but not in their brains. In female adult wasps, the virus grows in the tissues around their eggs. Once a wasp egg hatches inside a ladybug, the virus starts replicating inside it, too. The larva then passes on the virus to its host, and the ladybug develops an infection as well.

DcPV causes no apparent harm to the wasps, but the ladybug is not so lucky. The virus makes its way into the ladybug’s head, where it attacks brain cells and produces new viruses in pockets inside the cells. Many brain cells die off during the infection.

The researchers hypothesize that the virus is responsible for the change in the ladybug’s behavior. To get the ladybug to guard the wasp, the virus may partially paralyze its host, so that it becomes frozen over the parasite. Because the paralysis isn’t complete, the ladybug can still lash out against predators. But these may just be wild spasms in response to any stimulus. The bodyguard effect may grow even stronger as the infection robs the ladybug of the signals from its eyes and antennae. Closed off the world, its sole purpose becomes protecting its parasite.

The fate of a parasitized ladybug–to die or to walk away–may depend on how it handles a DcPV infection. In some cases, the virus may be fatal–possibly by triggering a massive immune response that kills not just the virus but the ladybug itself. In other cases, the ladybug’s immune system may eventually be able to clear the virus out of its system, letting its nervous system heal.

In either case, the bodyguard paralysis lasts long enough to protect the wasp while it develops into an adult. Whether the ladybug lives or dies doesn’t matter to the wasp–or to the virus. The new wasp carries a fresh supply of DcPV. If it’s a female, it will be able to use the virus to infect both its own young, and its ladybug slave.

In recent years, scientists have developed a deepening appreciation for the importance of our microbiome–of the bacteria and viruses that make our bodies their home. While some microbes invade our bodies, others reside inside of us and help keep us healthy. Parasitic animals have microbiomes of their own, and this new study suggests that they can use them for suitably sinister ends.

(For more information on the sophisticated tricks of parasites, see my book Parasite Rex.)

Last night at the National Geographic Society in Washington, I gave a talk with photographer Anand Varma about how parasites manipulate their hosts–the subject of my cover story in the November issue of National Geographic and Varma’s aesthetic obsession for the past couple years. Along with his gorgeous photos, Varma also showed off some lovely/creepy videos. I thought I’d share a couple of them with you. Pop them into full screen for full appreciation.

First off: Ophiocordyceps, a fungus that takes control of an ant. The fungus spores invade an ant’s body and then fill much its interior with tendrils. Under the fungus’s spell, the ant climbs up a plant and clamps down on the underside of a leaf. This movie, which Anand took in the Amazon working with Joao Araujo, a biology grad student at Penn State, shows the ant in its last hours, shot upside down for clarity. The fungus shoots a spike of spores out of the ant, which can then rain down on unfortunate ants below.

The second video shows how the white butterfly wasp takes over the cabbage butterfly caterpillar. A female wasp inserts her stinger into the host and injects dozens of eggs. They grow inside the caterpillar, which continues munching on leaves–leaves that now fuel the growth of the parasites inside. They chew their way out all at once, and yet they don’t kill the caterpillar. They prevent it from bleeding to death by thickening its bodily fluids and seal up their exit holes with bits of their own tissue. The caterpillar recovers from this strange birth and then spins a cocoon for the wasp larvae. It then sits atop its parasitic brood, fending off any animals that try to get at the wasps. At the end of the movie, you see the most dreaded of these enemies: another species of wasp that only lays its eggs in the larvae of the white butterfly wasp.

I’ve written the cover story for the new November issue of National Geographicabout the biology of parasite manipulation. I’ve been obsessed by this subject for a long time. (In my book Parasite Rex I wrote a chapter on this bizarre slice of reality). So it’s a huge delight to help give these mind-controllers the Nat Geo treatment: gorgeous pictures. When I wrote Parasite Rex, I gathered up what photos I could find, but none of them did the parasites justice. Anand Varma has journeyed to a number of countries to find the creepiest examples of this surprisingly common (and medical useful) phenomenon.

Anand and I will be speaking at the National Geographic Society in Washington DC about the story and photos on October 29. Please join us. Details are here.

As viruses go, Ebola has a grim star power. When a new outbreak hits, Ebola kills a high fraction of its victims, causing horrific bleeding along the way. The latest outbreak started in March in Guinea. As of today, the World Health Organization reported 231 cases and 155 deaths.

In order to better treat Ebola, Pardis Sabeti of Harvard and her colleagues have been analyzing the virus’s evolution. It turns out that Ebola is not some freakish new plague, but rather old. If that seems puzzling, a research scientist in Sabeti’s lab, Stephen Gire, has created this animation, which I’ve embedded below, to explain it.

Gire’s video is part of a contest being run by the National Institutes of Health. Check them all out and vote for your favorites. It’s great to see scientists being encouraged to explain what they do in a new medium like this. Wonderful things can evolve from this kind of experiment. A few years ago, for example, Brown University biologist Casey Dunn and his students started toying around with stop-action animation to tell stories of marine biology, and now their “Creature Cast” series is regularly featured on the New York Times web site.

Parasites can take many forms. Just this week, I’ve written about a giant virus that reproduces inside amoebae (and has survived being frozen 30,000 years in permafrost), along with a wasp that performs brain surgery to zombify hosts for its young. Viruses and wasps are radically different organisms–some would say that viruses don’t even deserve the label of organism. And they make use of their hosts in different ways. The virus sits inside a cell, manipulates its biochemistry to build virus proteins and DNA. The wasp, on the other hand, sips fluids inside a still-living roach, and builds its own proteins and DNA–and then becomes a free-living creature that can climb out of its host and fly away.

So why are they both parasites? The answer lies beyond the details of anatomy and molecules. It’s all about relationships.

Species can have all sorts of influences on each other. They can eat or be eaten, they can pollinate or steal pollen. But there’s one yardstick that scientists can use to measure all the variety in these interactions: the change that one species has on how many offspring the other can have. By that measurement, the differences between giant viruses and brain-surgeon wasps melt away. Each one is a disaster for its partner species. The viruses multiply inside amoebae until they burst. The roach lives until its wasp parasite is ready to depart. In each case, the relationship is good for the parasite (more offspring) and bad for the host (fewer).

When scientists look at life with this definition in mind, they can see a lot of parasites that might not look like parasites. We don’t think of birds as parasites–they’re too beautiful and not in the least bit creepy. But when a cuckoo pushes out the eggs of a reed warbler and puts her own in their place, and when the cuckoo chicks use all sorts of tricks to fool the reed warbler to feed them as if they were its own, we are seeing another parasite at work.

In the journal BMC Evolutionary Biology, a team of scientists in Finland describe another kind of parasite–one that doesn’t steal food or protein synthesis or even parental care. In the words of the scientists, these are “information parasites.”

These information parasites are, once again, birds. Lovely birds, in fact, known as pied flycatchers. And their victims are another species of bird, the great tit (twelve-year-olds at heart are allowed a few moments to get sniggers out of their system).

The pied flycatchers and great tits, both found across much of Europe, have evolved to the point where their existence is quite similar. They eat a lot of the same kinds of food, get killed by the same predators, and even choose the same sites for their nests. This similarity leads to a fair amount of competition, sometimes quite violent. If a bird from one species flies into a crevice to check out a potential nest spot, only to find the other species there, the two birds will fight–sometimes to the death.

The two species aren’t identical, though, and there a couple differences that are particularly intriguing.The great tits build their nests earlier in the year, and the pied flycatchers have a habit of paying visits to great tit nests before building their own.

In recent years, the Finnish researchers have found a likely reason for these visits. The pied flycatchers are gathering intel. They inspect the nests of great tits to help them decide where they will make their own nests. One piece of information they’re interested in is the number of eggs are in a great tit’s nest. If a nest is loaded with eggs, it’s probably a good place for a pied flycatcher to make its own nearby.

The great tit suffers for letting the pied flycatcher get this information. Now a rival bird sets up house on the same territory and starts to compete for the same food. The researchers have found that great tits that attract these neighbors end up with fewer nestlings as a result. The pied flycatchers, on the other hand, have more success in reproducing because they build their nests on good real estate. One species benefits, and one suffers. But the benefit doesn’t come from cockroach innards or cell proteins. The pied flycatcher is stealing information.

Once parasites evolve a strategy for taking advantage of a host, the host generally evolves defenses. Immune systems recognize pathogens and destroy them. The hosts of some wasps will fly away or fight off their attacker. If pied flycatchers really were information parasites, then great tits might evolve defenses to safeguard their information.

When great tits are laying eggs, they search for sheep hair and other materials to keep the eggs covered. It’s not clear why they bother. You could imagine that the covering is a blanket to keep the eggs warm. But the birds don’t bother to keep the eggs covered once they’re all laid and the embryos start to develop. So it’s possible that they’re doing something else with the hair.

One thing that the hair does is hide the eggs. The Finnish scientists wondered if the great tits use hair to hide information from flycatchers. To find out, they ran an experiment.

They put a decoy of a pied flycatcher five meters from great tit nests and played a recording of a pied flycatcher singing for five minutes. The next day, they collected the hair in the nests. The scientists then ran the same experiment, but with decoys of cedar waxwings–birds that live alongside great tits but don’t compete with them.

The great tits responded to pied flycatchers by adding over 40% more hair on top of their eggs than they would otherwise. The scientists concluded that the birds hide the eggs when pied flycatchers show up so that the pied flycatchers won’t see just how well the great tits are doing. Seeing what looks like a meager nest, the pied flycatchers will be more likely to move on.

When hosts evolve defenses against parasites, parasites sometimes evolve counter-defenses. When flu viruses infect a cell, for example, the cell can respond by making an anti-viral protein called interferon. The interferon guides the cell to chop up the invading virus genes. But flu viruses have proteins that block interferon.

Do information parasites have their own counter-defenses? The scientists don’t offer any solid scientific evidence in their new report, but they do mention that they’ve seen something odd. They’ve seen pied flycatchers sneak into great nests and pull hair from the eggs. That may seem like a pointless exercise, since pied flycatchers don’t use hair on their own nests. It’s possible that they’re just trying to steal some reliable information.

When I first started writing my book on the triumph of parasites, I burrowed into the science and was stunned at how many ways there were to be a parasite. Eventually, the bottom just fell out. This is the first time that I’ve become aware of the concept of “information parasites,” but I suspect it won’t be the last.

If you’ve never met the emerald jewel wasp, let me introduce you to my little friend.

The wasp (Ampulex compressa) lives the first stage of its life as a parasite, growing inside the body of a living cockroach. That’s absorbingly horrific on its own, but how it gets into the cockroach in the first place is an especially gruesome delight. Its mother has to play neurosurgeon.

A female wasp seeks out a cockroach host and ambushes it. She inserts her stinger into its thorax and delivers a paralyzing shot of venom that immobilizes the insect for a few minutes. She pulls her stinger out and then delivers a second injection. This one goes into the cockroach’s head, delivering more chemicals to two sites in the brain of the host.

Image copyright Quade Paul

The result is a cockroach zombie. The neurosurgically altered victim recovers from its paralysis but now lacks the will to flee or fight. The wasp pulls on an antenna and leads the roach, like a dog on a leash, into a burrow. There she glues an egg to the underside of the roach. She leaves the burrow and seals it shut. In the darkness, the roach stands motionless as the wasp larva hatches from its egg and chews a hole into its side. The wasp feeds through the hole for a while, and then slithers inside. Later, it pops out as a full-grown adult.

Image by Ram Gal

At Ben-Gurion University, Frederic Libersat and his colleagues have been studying the emerald jewel wasp for over 20 years, and they continue to learn new things about it. In the journal PLOS One, they’ve now published previously unknown details about the creepiest part of the wasp’s attack: its injection of zombie drugs into the cockroach brain.

To appreciate just how tricky this can be, consider what it takes for doctors to deliver drugs to a human brain. They scan the patient’s brain to map its anatomy in three dimensions. Then they put their patient’s head in a cage, drill a hole in the skull, and then slowly push a tube into the brain. A wasp does much the same thing in about a minute, without ever glancing at a brain scan of its victim.

Some days I wish I was a jewel wasp. Photo source: http://neurosurgerycns.wordpress.com

They pull off this feat with their extraordinary stinger. It measures 2 millimeters long, enabling the wasp to insert it into the roach’s neck and snake it up to the brain. The tip of the stinger has two sets of valves. One set hold the equipment for laying eggs, and the other set hold the equipment for delivering venom. The valves interlock in a tongue-and-groove arrangement so that they can slide over each other, allowing the wasp to lay an egg or deliver a sting with the same organ.

The stinger, the scientists also found, are studded with little bumps–some shaped like bells, others like domes. Each bell-shaped bump has a touch-sensitive nerve ending inside it, while the dome-shaped bumps have a touch-sensitive nerve ending along with four or five chemical-sensing ones.

To see what those bumps are doing, the scientists put electrodes inside the nervous system of wasps and then pushed the stinger against rubbery lumps meant to simulate a roach’s brain. The wasps’s nerves crackled with activity when the bumps on the stinger tip pushed along a lump. This response suggests that the wasp uses its stinger to feel its way through the roach’s brain.

To see if this was true, the scientists stripped the stinger bumps off of wasps and then let them attack a cockroach. The average time the wasps spent probing the cockroach brain shot up from just over a minute to nearly 20 minutes. That’s what you’d expect if the wasps suddenly were unable to find their way inside a cockroach brain.

The scientists then ran another type of test, presenting healthy wasps with roaches that they had altered in various ways. They took the brains out of some roaches and left them with hollow heads. In other cases, they swapped the brain with a rubbery lump (some lumps were hard and others soft). In still other cases, they injected a toxin into the brains of the cockroaches that silenced their neurons. And in still other cases, they insert scissors into the roaches’ heads and snipped up the brains into a homogenous mush.

The scientists found that some–but not all–of these altered roaches posed a challenge to the wasps. If a wasp stung a roach without a brain, she spent over ten minutes probing its head. A soft rubbery lump also stretched out the time the wasps stung their hosts. And after that long struggle, the wasps withdrew their stinger in defeat, without delivering their zombie venom.

But when the wasps encountered a hard rubbery lump–a lump with the same texture as a brain–they spent just a minute poking the cockroach, after which the scientists found venom in the victim’s head.

Nor did the scientists find any change when the wasps were presented with roaches whose brains had been silenced–suggesting that the wasps don’t sense electrical activity to guide their stinger. On the other hand, a shredded brain left the wasps groping. That result suggests that the wasps need to do more than just feel the roach brain–they need to feel different parts of the brain in order to get where they need to go.

Taken together, these results offer a picture of an exquisitely evolved sensory organ–one adapted not for some all-purpose perception, but solely to navigate the interior of a cockroach’s brain by sense of touch. The full magnificence of this sensory organ may yet to be revealed, however. In their new study, Libersat and his colleagues didn’t determine what the chemical-sensing dome-shaped bumps are for.

Do the wasps taste their way through a cockroach brain? It’s possible–but perhaps the dome bumps provide it with other kinds of information. The scientists speculate that the dome bumps may taste the wasp’s own venom as it’s released into the roach’s brain, so that the parasite can carefully control how much she delivers to her victim (this is neuropharmacology, after all). Or perhaps the wasp can taste the flavor of larva of other species of parasites–in which case she may abandon the already-infected cockroach for a fresh host.

If someone answers that question, I guarantee to let you know. In the meantime, here is a video of a talk I gave for TED-Ed in 2012 about the jewel wasp. And if that’s just not enough for you, check out my book Parasite Rex.

In case snakes weren’t enough of a fright-fest for you this Halloween, here’s a video that I narrated for National Geographic about one of nature’s spookier creatures. (One of many, as I explain in Parasite Rex.)

Life is rough for parasites. Say you’re a tapeworm that only lives in the gut of one species of shark. You start out as an egg inside an adult tapeworm. Your parent releases you and a bunch of other eggs from its body, and its shark host shoots you out of its own body. Now you float in the vast ocean, stretching out on all sides. You are not made for the free-living world. If you don’t get into another host, you will never reach adulthood. Not just any host, but a fish. And not just any fish, but one species of shark. Chances are good, in other words, that you’ll die.

The miserable odds for individual parasites can potentially drive the evolution of something remarkable: the ability of parasites to manipulate their hosts. By controlling their hosts, the parasites can raise their odds of surviving and reproducing.

Scientists have gathered a number of examples of host manipulation over the years. I dedicated a chapter of my book Parasite Rex to some of them, and a group of scientists published a whole book on the topic last year. A lot of these parasites are cool just in and of themselves, whether they infect caterpillars or spiders, but inevitably people want to know whether parasites control us. I put it down to a combination of our species’s narcissism and love of zombie movies. There are a few potential cases of parasites influencing–if not outright manipulating–human behavior. And the most intriguing one of them all involves a single-celled parasite called Toxoplasma gondii.

Toxoplasma gondii forms cysts in people’s brains. Unless their host has a weak immune system, their cysts cause no apparent harm. But they make up in numbers what they may lack in deadliness. Perhaps a billion or more people carry Toxoplasma cysts in their brain. They pick up the parasites in the soil, undercooked meat, or cat litter.

It’s in cats that the Toxoplasma life cycle gets its start. The parasites mate in the intestines of cats and then produce egg-like offspring, which are passed out with cat droppings. The durable eggs can stay viable for months as they wait for their next host–which can be any species of mammal or bird. Those hosts swallow the parasites, which migrate out of their gut and wander their body; the ones that make it to the brain form protective cysts and play the waiting game again. Only if they can get back into a cat’s gut will they be able to take the next step in the Toxoplasma life cycle.

As other cases of parasite manipulation came to light, some scientists wondered whether Toxoplasma might have some tricks of its own. After all, there’s one obvious opportunity for increasing its odds of getting into cats: make its host easier for cats to catch.

Starting in the late 1990s, a number of researchers published evidence indicating that the parasite does, in fact, do this. Most of the work has been carried out on rats and mice. In a number of experiments, infection with Toxoplasma appears to make the rodents less frightened by the smell of cat urine. Some studies even hint at an attraction to the scent of their killer. (I’ve written about some of the research in recent years here and here.)

“In our opinion,” the authors declare, “the accepted dogma that T. gondii manipulates host behavior to increase transmission to cats, tells an appealing story but does not stand up to scrutiny.”

They make their way systematically through the published record of experiments on Toxoplasma. They observe that the parasites produce a range of effects on the behavior of their hosts. In some studies, animals become more active, while in others they become less active, and in others they experience no change at all. In one study, scientists found that Toxoplasma impaired a host’s ability to learn, and in another, it didn’t. The same split in results turns up in tests on memory, a preference for exploring new things, time spent near cat urine, and anxiety.

The scientists also attack the elements that make up the manipulation hypothesis. Just because a parasite does something that appears to make it easier prey does not mean that natural selection produced that change to improve its odds of completing its life cycle. Toxoplasma could be altering its hosts as a side effect of infection, not as an evolved adaptation. The authors note that another single-celled parasite called Eimeria also robs mice of their fear of cats, despite the fact that its life cycle takes it from mouse to mouse, not mouse to cat.

If natural selection really had been at work here, it would be necessary for manipulations to actually increase the number of offspring Toxoplasma produced. But no one has ever done a large-scale trapping experiment to see whether cats catch more Toxoplasma-infected prey than healthy ones. This sort of experiment has been done for other species. In an experiment on fluke-infected fish, researchers found they became easier targets for birds because they jumped around near the surface of the water.

On the other hand, some behaviors that seemed like they ought to make hosts more likely to be killed turned out not to. A tapeworm called Hymenolepis dimunata alternates between beetles and rats. When it infects beetles, they spend more time out in the open, where they ought to be easier for rats to find and eat. Despite such expectations, scientists found that infection didn’t actually raise the odds of a beetle getting killed. In the case of Toxoplasma, rodents may lose their fear of cat urine but might still avoid other scents from their predators, such as the smell of cat fur.

The Australian scientists also point out that Toxoplasma has a more flexible life cycle than it’s often given credit for. It has to get into cats in order to sexually reproduce. But it can also clone itself in other species. The parasite can even spread from mothers to their offspring. When scientists survey the DNA of Toxoplasma, they see evidence for a lot of cloning, and not a lot of mixing genes through sex. If the parasite isn’t moving much between cats and their prey, the natural selection for manipulation should be weak.

A lot’s been made of the fact that Toxoplasma winds up not just in rat brains, but in human brains. Some scientists have argued for a whole host of changes to behavior in people who carry the parasite. It’s tempting, for example, to see “cat ladies” as being in the thrall of cat-infecting parasites. The critics think all this speculation is completely unwarranted at this point.

“Given that research into human behavior is based at least partly on findings in rodents,” the authors conclude, “it is vital that we have a good understanding of how rodent behavior is affected by T. gondii, before we extrapolate to other species.”

I reached out to some of the scientists who have done the most prominent work advancing the manipulation hypothesis. While they all agreed that scientists should be careful to avoid assuming adaptations that may not actually exist, they dispute a lot of the claims made by the Australian critics.

“I firmly believe Toxoplasma is a clear case of actual manipulation and that their attempt to dismiss this is a little too naïve and simplistic,” says Joanne Webster of Imperial College. Webster herself is no “manipulation fundamentalist,” as it were–she was the one who did the beetle experiment that the Australian critics use as evidence against manipulations. But she thinks that the evidence for Toxoplasma is strong, and the criticism against its power to manipulate are weak.

Mathematical models of evolution, for example, show that it’s not necessary for there to be a huge boost in cat attacks in order for natural selection to favor manipulation. And while it’s true that Toxoplasma doesn’t need sex to reproduce, sexual reproduction in the long run has many advantages–such as mixing genes together into better combinations.

Webster agrees that it would be great to see whether cats are more likely to kill infects prey than uninfected ones, but that’s a hugely challenging undertaking for all sorts of reasons (such as the rules about animal welfare). Michael Eisen, a Berkeley researcher who has done experiments on Toxoplasma in mice in recent years, put it this way:

It’s an almost impossible experiment to do right. Are you going to infect mice and release them and a control group and see which get eaten? Where would you do that? How would you know the results wouldn’t be different in a different setting?

As for the different results from some studies on Toxoplasma infection, Webster argues that a lot of that may come down to the fact that scientists have run some experiments on lab rodents and others have studied wild ones. Lab animals have been bred for decades away from their natural threats–including cats. If these differences are accounted for, Webster still sees the evidence for manipulation as being strong.

Eisen, on the other hand, thinks that scientists have yet to do enough experiments to make any strong statements about Toxoplasma. “We’re still far away from having done truly definitive studies to characterize the behavior itself,” he said. “Let’s talk about this before we start calling Toxo the parasitic king of behavior manipulation.”

Still, he agrees with Webster that the critics make a weak case when they try to downplay the importance of cats to Toxoplasma’s long-term survival. If Toxoplasma can do so well without having sex inside of cats, he asks, why does it still carry so much genetic machinery for having sex and producing offspring? Eisen calls this argument from the critics “very poor evolutionary thinking.”

Finally, I got in touch with Ajai Vyas of Nanyang Technological University. He’s done some of the most detailed work on how Toxoplasma affects the brains of rodents, finding it zeroes in on emotional circuits. Vyas pointed out that scientists have debated for a long time how you can tell whether the effects of a parasite are an adaptation for manipulating their host. A few criteria have emerged. Is the effect complex? Is it something that well-fitted to a parasite? Does it turn up in different parasite species, suggesting natural selection has favored it repeatedly. By these standards, Vyas argues, it makes sense to look at Toxoplasma as a manipulator.

But it’s also important to bear in mind that the cats and rodents that we see today–even in the so-called wild–are living in a human-dominated world. Both predator and prey in this case have benefited from our company; we’ve moved them around the world, we’ve given them shelter, and we’ve given them–intentionally or not–an abundant supply of food. The manipulations that Toxoplasma originally evolved may have been less ambiguous before its hosts underwent so much rapid change.

“It could be a historical legacy rather than a present adaptation,” says Vyas. “I am not yet clear about this.”

Millions of years ago, some bats gave up their old habits of hunting for insects and tried something new: drinking blood. These creatures evolved into today’s vampire bats, and it’s mind-boggling to explore all the ways that they evolved to make the most of their sanguine meal.

A lot of the adaptations are easy enough to see with the naked eye. Vampire bats have Dracula-style teeth, for example, which they use to puncture the tough hide of cows. When they open up a crater-shaped wound, they dip in their long tongue, which contains two straw-shaped ducts that take up the blood.

Finding these prey has led to another remarkable adaptation that you can see–at least if you’re a scientist who studies how vampire bats move. Like other bats, they can fly, but on top of that, they can also walk and, yes, even gallop. Here is a video of a running vampire bat made by Dan Riskin (see this Loom post for details). Of the 1200 or so species of bats, vampire bats are among the very few that can move quickly on the ground.

But vampire bats have many other adaptations for drinking blood that are invisible. They use their combined senses–long-range vision, a sharp sense of smell, acute hearing, and echolocation–to find their victims. In their noses, they even have heat-sensitive pits that detect the heat of warm-blooded animals. Once they land on an animal, they apply those pits to the skin to locate capillaries full of hot blood close to the surface.

Photo by Bruce Dale/National Geographic

When vampire bats dip their tongue into a wound, they don’t just draw out blood. They also put their saliva into their victim. And in this liquid are still more invisible adaptations for a blood-feeding life. Vampire bats, you see, are venomous.

This may sound odd. That’s because we usually think of venom as a chemical an animal sticks in your body to cause you pain or death. But biologists define venom more broadly than that: it’s a secretion produced in a specialized gland in an animal, which is delivered to another animal by inflicting a wound, where it can disrupt its victim’s physiology.

Snake venom, the sort we’re all most familiar with, can disrupt physiology to the point of death. And it does so in several ways–jamming neurons, for example, or causing tissue to rot. But other animals that don’t set out to kill their victims also produce venom. Vampire bats, for example, don’t want eat a whole cow. They just want to take a sip.

Unfortunately, drinking blood has some drawbacks. Vertebrates come equipped with lots of molecules and cells that plug up wounds. As soon as they sense even a tiny tear in a blood vessel, they start making clots to staunch the flow.

What’s most striking about vampire bat venom is how it goes after its victim from so many directions. Blood clots develop through a series of reactions that involve a chain of enzymes. Vampire bats produce different proteins to go after different enzymes in that chain. Platelets, which are cell fragments, also clump around wounds to help heal wounds. Vampire bats make separate compounds that attacks platelets.

To make their venom cocktail, vampire bats have repurposed old molecules for new jobs. When any vertebrate formed a blood clot to stop a wound, it needs to break that clot down once the wound is healed. An enzyme called plasminogen activator creates a supply of molecules called plasminogen, which chops up the clots. Vampire bats produce plasminogen activators in their blood for this job. But they also produce an extra supply in their mouth glands. When the plasminogen activators get into a wound, they use the victim’s own plasminogen to keep the blood flowing.

Once bats borrowed plasminogen activators to use in their venom, the molecules became better adapted to that new job. Normal plasminogen activators get cleared from the blood stream by other enzymes. That’s important for our survival, because otherwise they would hang around and make it hard to form new clots. Vampire bat plasminogen activators have a slightly different shape that shields them from their victim’s enzymes.

Together, these molecules are so effective that a cow will keep bleeding long after a vampire has flown away. While scientists have been studying vampire bat venom for decades, they’re still finding new molecules in the cocktail. The authors of “Dracula’s Children” applied a new method to the search. They caught two vampire bats and cataloged all the genes that were highly active in their mouth glands. The scientists then identified the genes and studied the properties of the proteins they encoded. They discovered dozens of new proteins. Some of them kill microbes, keeping the bat’s food supply clean. Some expand blood vessels, increasing the flow into the wound.

When a cow gets attacked by a vampire bat, it’s not entirely helpless. Ranchers have noticed that when bats feed over and over again on their herds, the cows bleed for a shorter period of time. Scientists have found that this happens because the immune systems of the animals learn to recognize some of the venom molecules and attack them. In the new study, the researchers found venom molecules that can ward off the immune system. But the venom itself is evolving to escape the immune system’s recognition, taking on new shapes that may allow them to go unnoticed.

Reading “Dracula’s Children” gives me a potent sense of deja vu. I recently wrote a feature about ticks for Outside, and in the research for the piece I learned all about how ticks produce saliva loaded with proteins that, among other things, open blood vessels, use our own molecules to break up clots, and do many of the things that vampire bat venom does.

Vampire bats are what you get if you turn a mammal into a tick. And I mean that as the highest compliment.

(For more on the convergences of parasites, see my book, Parasite Rex.)

I’ve written about a lot of parasites over the years, but for some reason I haven’t gotten around to one that’s intensely familiar to suburbanites: the tick. Recently, Outside asked me to write a feature about these blood-sucking creatures–exploring their chilling sophistication as blood-suckers and their disturbing ability to spread pathogens. Fortunately (if that’s how you want to think about it) I live in Tick Central, otherwise known as Connecticut. To report on Lyme Disease, I can drive up the road to Lyme. My story is in the June issue of Outside. Check it out.

NOVA put together a video, embedded below, about one of those animals that you have to keep persuading yourself is real, a parasitic crustacean that lives inside the mouths of fishes, eating–and then taking the place of–its host’s tongue.

I can vouch for these beasts, having written about them off and on since I first encountered them in my research for Parasite Rex—most recently on the Loom last year. But I was not aware that it’s the female that wins the Oscar for best performance as a fish tongue. The males just hang out around the gills of the fish and then–yep–mate with the pseudo-tongue.

This discovery led me to wonder about the latest research about tongue-eating isopods. I came across a 2012 master’s thesis by Colt William Cook of the University of Texas, which confirms what you see in the video–that the parasites are born as males, and then when they enter a fish, one turns female. This switch only occurs if there’s no female already installed in the host–otherwise, the males stay male. As this transformation takes place, Cook adds, the female’s body grows enormously. Its eyes shrink, since it no longer has to hunt for a home. Its legs stretch out, to help it anchor itself in the mouth.

Courtesy of Matthew Gilligan

After one of the males mates with the female, she gives birth to a brood of live male parasites. For their first few days, Cook found, they search madly for another host (each species of parasite seems to only live in a single species of fish). They sniff for the scent of their host, and if a shadow passes overhead when the odor is strong, they shoot upwards through the water. They burn through a lot of energy in the process; if they fail to find a host in the first few days, they settle down and hope they can ambush a fish that happens to be swimming by. It’s a hard way to start your life, and it may explain why several males will huddle inside a fish with only a single female in the offing. Looking for another fish with a single female parasite might be a less promising strategy than competing with the males you’re with.

Of course, these rules may only apply to the species that Cook studied, which infects Atlantic croakers off the coast of Florida. The full diversity of these tongue parasites is probably enormous. A 2012 study puts the total species at 280, but that’s just known species. A team of scientists from Annamalai University in India recently did a survey of the parasites in fishes off the coast of India. Before their study, scientists knew of 47 species of parasites in Indian waters. In just nine fishes, the scientists discovered ten new parasite species. I’d wager that some of the species waiting to be discovered will prove to be even more surreal.

In 1980, a man walked into the Royal Perth Hospital in Australia, complaining that he was tired. He had been tired at that point for two years. The man’s medical history offered no good clues–at 44, his only indulgence was a glass of white wine at dinner each night. His doctors pushed and poked until they discovered his liver was swollen. Yet he showed none of the symptoms you’d expect from cirrhosis or liver cancer. The cause of the man’s trouble only became clear when the doctors got the report on his stool. It contained eggs from an animal known as Schistosoma mansoni–otherwise known as the blood fluke.

Blood flukes are parasitic flatworms. They get their start living in snails, which shed the parasites into the surrounding water. If you go wading into a blood fluke-infested pond, the missile-shaped flukes will sniff their way to your skin and drill in. Once they reach a blood vessel they surf the sanguine tide until they reach your intestines. They take up residence in the blood vessels there, producing eggs that they nudge into the intestinal walls. The eggs get washed out of the body with their host’s stool, perhaps to infect a freshwater snail. Sometimes, however, the eggs get swept off in the wrong direction and wind up in the liver, where they cause chronic inflammation.

Getting blood flukes (the disease is known as schistosomiasis or bilharzia) is, sadly, nothing special. Two hundred million people suffer from infection with Schistosoma mansoni or a related species of blood fluke, Schistosoma haematobium. But the case of the man at the Royal Perth Hospital was singular in one respect. In order to get infected with blood flukes, you have to go to the places where its snail hosts live. And Australia is not one of those places. The man had, in fact, traveled to East Africa, where the blood flukes are common. But he hadn’t been there in 31 years.

This was remarkable, and more remarkable than you might think. It didn’t mean that the blood flukes had taken up residence in the man’s body and had produced 31 years of new generations. Remember, the eggs cannot develop inside a human body. They have to reach fresh water to hatch, and if they can’t find a snail to invade, they die. The tired man in Australia had been carrying the same blood flukes with him that he had picked up in Africa. These parasites were themselves at least 31 years old.

The many years that a blood fluke can spend in a human host are striking, and all the more striking the more you contemplate how they spend those decades. Most species of flatworms are hermaphrodites, with both eggs and sperm. Blood flukes are either male or female. The females are thin and small. The males are larger, shaped like a canoe. At one end of their body, they had a mouth for drinking blood and a giant sucker. In their human host, female blood flukes select their mates and fit themselves into the trough of the male’s body. There they will remain, getting nourishment from their mate, along with the sperm necessary to produce their eggs. Blood flukes will spend years in this monogamous union, although sometimes they will get divorced and seek a new mate.

In all that time, the blood flukes manage to survive inside enemy territory. These are not microscopic creatures; they can get to be a centimeter long. Yet the immune system of their host typically ignores adult blood flukes. How they manage to escape notice–instead of getting rejected like a transplanted organ–isn’t yet clear. The parasites probably evade destruction by producing camouflage in the form of human-like proteins.

This discovery is the work of Philip Newmark of the University of Illinois and the Howard Hughes Medical Institute and his colleagues. Newmark–like many other scientists–has spent years studying free-living cousins of blood flukes called planarians. Planarians can reproduce in a manner that seems to defy the rules of zoology. They simply split in half, and each half then regrows the rest of its body.

Scientists can regrow new planarians from tiny cuttings, complete with muscles, intestines, nerves, and the many other organs that are necessary for a full-blown flatworm. We’ve known about this power of regeneration for centuries, but it always bears appreciating anew. Imagine that someone cut off your ear and tossed it on the ground, where it promptly grew into a complete copy of yourself–complete with a new brain.

This power makes planarians an object of fascination for cell biologists. They’ve searched these flatworms for the secrets of their renewal. It appears that their bodies are sprinkled with unusually flexible stem cells called neoblasts. These cells can travel the planarian body to wherever they’re needed. Once they arrive, they start dividing quickly and differentiate into any tissue the planarian requires.

Our bodies can also regenerate themselves, albeit on a far more modest scale. As adults, we carry small collections of stem cells that can produce new tissues. They heal a gash by producing new skin cells. In the intestines, they produce new lining to replace sloughed-off cells. Stem cells in bone marrow rejuvenate our blood supply. Stem cells may also be important to the workings of the brain. But in these cases, the stem cells have only a narrow scope. They can only develop into a few cell types. We can regenerate skin and even a lobe of our liver, but we can’t regrow an eye or a hand. Studying planarians allows scientists to discover some of the signaling molecules that might be able to trick our own stem cells into more dramatic rebirths than they can manage on their own.

Newmark and his colleagues asked themselves one of those questions that seems so obvious in hindsight that you have to wonder why no one asked it before. Given that planarians and blood flukes are cousins, do blood flukes have this same power of regeneration? It’s an easy question to ask, but a vexingly hard one to answer. Planarians live cheerfully in a lab tank, but blood flukes require snails and mammals to complete their life cycle. Newmark and his colleagues have helped make it easier to study blood flukes in recent years; for example, they’ve developed a toolkit of molecules they can apply to blood flukes to probe their cells.

The neoblasts in planarians are constantly dividing. So Newmark and his colleagues started their search for similar cells in blood flukes by looking for signs of proliferation. As a cell multiplies, it makes DNA, and chemists have found that a compound called EdU can get taken up in the structure of new DNA. Newmark and his colleagues doused blood flukes with EdU and then inspected the parasites under a microscope to see if any cells had taken it up. They found proliferating cells sprinkled throughout the blood fluke body.

Newmark and his colleagues teased out some of the multiplying cells and gave them a closer look. They bore a striking resemblance to neoblasts, not just in their structure, but in the activity of their genes. All these clues pointed in the same direction: the proliferating cells in the blood flukes seemed a lot like neoblasts from planarians.

To watch these cells in action, the scientists infected mice with blood flukes. Then they injected the mice with EdU, which the parasites took up in their proliferating cells. Those cells then migrated through the body of the blood flukes. Some headed to the intestines of the parasite, while others headed to the muscle. There the cells divided into new cells, rejuvenating both kinds of tissue.

Newmark and his colleagues conclude that blood flukes have flexible stem cells akin to the neoblasts of planarians. It’s possible, they suggest, that these stem cells help blood flukes live so long. They may rejuvenate the parasites after they’ve been attacked by the immune system, or allow them to recover from a dose of anti-schistosome medicine. And as the blood flukes get old, the cells can be a fountain of youth, rejuvenating their tissues.

If these cells are indeed important to blood flukes, then we would do well to learn how to manipulate them. Newmark and his colleagues noticed that one of the genes switched on in the neoblast-like cells belongs to a family of signaling genes that are important to keep stem cells multiplying. They figured out how to make a drug that blocks that gene in blood flukes. In the drugged parasites, the neoblast-like cells slowed down.

If these flexible stem cells really are essential to the longevity of blood flukes, then this drug could be a powerful weapon against them. To fight against some parasites, we may have to take away their fountain of youth.

(For more information on blood flukes and other marvels of the parasitic world, see my book Parasite Rex.)

Citizens and scientists alike feared that whatever was altering the frogs–pesticides perhaps–was also having an effect on humans. But researchers didn’t find any compelling link between frog deformities and humans diseases such as cancer. In fact, within a few years it looked as if the frogs were getting their legs naturally–through the manipulations of a parasite.

The parasite in question is a flatworm called Ribeiroia. It starts out life in snails. It grows and reproduces inside the snails, which it castrates so that they don’t waste time on making eggs or looking for a mate. In its castrated host, the parasite produces a new generation of flatworms that can escape the snail and swim in search of a vertebrate host. They typically infect fish or tadpoles. When they invade tadpoles, the parasites bury themselves in the tiny buds that will eventually grow into legs.

As the frogs develop their legs, the parasites wreak havoc. In some frogs they will stunt the growth of a leg, leaving it a stump. In other frogs, a developing leg forks in two. A single frog may even sprout a dozen legs. It’s not clear yet how the parasites manage this feat, but one recent experiment offers a clue.

In order for a limb bud to develop properly, its cells have to produce certain molecules. The molecules spread out across the limb bud, causing other cells to make other molecules, to grow faster, to die off, and to do all the other things required to make a limb. (See my article in the New York Times for more on this process.)

One of the crucial molecules for building legs is a version of Vitamin A, known as retinoic acid. Dorina Szuroczki and Nicholas Vesprini of Brock University and their colleagues found that before the swimming parasites find a tadpole, they are producing retinoic acid. Once they’re buried in the frog’s limb bud, their level of retinoic acid drops. Meanwhile, the level of retinoic acid in the limb bud shoots up 70 percent. All of these findings are consistent with the idea that the parasite is injecting limb-deforming drugs into their host.

The deformities of the frogs are not merely a side effect of their getting sick, in other words. They’re part of a strategy that the parasite uses to advance its life cycle. To understand why this would be so, you have to bear in mind that the frog is just a way station for the parasites. They cannot mate or reproduce in frogs. Instead, they have to wait to get into a bird, where they take up residence in the gut and produce eggs that are shed by their host. And they can only make that trip if the frog they inhabit is caught by a bird. Some frogs get eaten, and some don’t. A parasite in a frog that escapes death by bird will die without reproducing.

Brett Goodman and Pieter Johnson of the University of Colorado ran an experiment in 2011 to see what effect the limb deformities have on the frogs. They infected frogs in their lab and then compared their performance to healthy animals. The scientists found that the jumps of malformed frogs were 41 percent shorter than those of healthy frogs. They swam 37% slower and had 66% less endurance. They tried just as often to catch crickets, but they caught 55% fewer insects.

Goodman and Johnson then studied the frogs in the wild, observing how well they survived in a pond in California. Surprisingly, extra legs had no significant effect on the survival of the frogs–as long as Goodman and Johnson kept their ponds free of predators. The deformed frogs could still get around well enough to find enough food to stay alive. But in ordinary ponds, the parasitized frogs were at grave risk. Over a fifth of them died every two weeks, and when a given generation of frogs became adults, there were almost no deformed frogs left among them. Instead, they had delivered their parasites to their next home.

The discovery of this parasite manipulation was not the end of the story, though. Even though Ribeiroia has probably been infecting frogs long before people showed up in the United States, the level of infection might be influenced by a number of factors. Johnson and his colleagues have found, for example, that frogs that live in water contaminated with high levels of fertilizers were more likely to be infected with Ribeiroia. Pesticides can kill off the parasites, some studies show, but they also lower the defenses of the frogs, which may lead to higher infections.

In this week’s issue of Nature, Johnson and his colleagues now offer evidence for another factor in the success of leg-deforming parasites: biodiversity.

Credit: D. Herasimtschuk, Freshwaters Illustrated

For some years now, a number of ecologists and parasitologists have developed the idea that biodiversity protects against disease. The notion is this: parasites in search of a new host sometimes end up in the wrong species. A bird flu virus that gets into a bird, for example, can make billions of new viruses that are shed in the bird’s droppings, which can then infect other birds. But bird flu sometimes gets into a human and cannot spread any further. The more species in an ecosystem, the argument goes, the more likely parasites are going to hit a dead end and get diluted. In low-diversity ecosystems, parasites will be more likely to hit the right host, make more copies of themselves, and cause more disease.

It’s a very influential idea, but, like many ideas in ecology, very hard to test. Johnson and his colleagues realized that Ribeiroia offers a very good opportunity to do so. The parasite only manages to trigger limb deformities in some of its hosts, and it has more success in some amphibian species than others. What’s more, each pond occupied by the parasite and its hosts is like a test tube in which the experiment is replicated. Johnson and his colleagues have visited 345 sites in California wetlands to examine Ribeiroia and its hosts. All told, they studied 24,215 amphibians and dissected 17,516 snails.

In these wetlands, the parasite is most successful when it infects Pacific tree frogs. But it can infect other frog species and even the salamanders that live alongside the frogs. Johnson and his colleagues found that in ponds with high biodiversity–up to six species of amphibians–the parasites did much worse at getting transmitted than in low diversity ponds. This was no minor difference: there was a 78.5% decline in deformed frogs in high-diversity sites. To test this pattern, Johnson and his colleagues put groups of amphibians into tanks along with infected snails. The frogs in high-diversity tanks had half the parasites as the ones in low-diversity tanks.

It seems, then, that we can add low biodiversity to the list of factors that can produce a flurry of frog legs, along with pesticides and fertilizer. Johnson also suspects that the snails are important too. As the parasite population grows, it castrates more and more snails, until their population crashes. Once the snails become scarce, the parasites become scarce, too, giving the frogs a break. Unfortunately, no one has yet conclusively shown that any of these factors has driven a long-term change in frog deformities of the sort that made headlines in the 199os.

Nevertheless, this study is important for a few reasons. For one thing, frogs are in big trouble these days. Species are winking out around the world, and diseases appear to play a big part in their demise. Biodiversity itself may defend the frogs against dangerous outbreaks.

It also tells us something about our own well-being. We don’t have to worry about frog flatworms getting into our bodies and causing us to sprout extra legs, thank goodness. But many other pathogens that do make us sick also lurk in other species, such as West Nile virus and hantavirus. And the more species that can dilute those pathogens, the healthier we’ll be.

[For more information on the link between biodiversity and human health, see David Quammen’s new book, Spillover. I write about parasite manipulations in Parasite Rex.]

Who We Are

Phenomena is a gathering of spirited science writers who take delight in the new, the strange, the beautiful and awe-inspiring details of our world. Phenomena is hosted by National Geographic magazine, which invites you to join the conversation. Follow on Twitter at @natgeoscience.

Ed Yong is an award-winning British science writer. Not Exactly Rocket Science is his hub for talking about the awe-inspiring, beautiful and quirky world of science to as many people as possible.
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